The project was led by Nima Rahbar, the Ralph H. White Family Distinguished Professor and head of the Department of Civil, Environmental, and Architectural Engineering. His team created ESM using an enzyme that helps turn carbon dioxide into solid mineral particles. These particles are then bonded together and cured under gentle conditions. The process allows the material to be shaped into structural components within hours.

Conventional concrete must be produced at very high temperatures and can take weeks to fully cure. In contrast, ESM forms quickly and leaves a much smaller environmental footprint.

Cutting Emissions by Capturing Carbon

“Concrete is the most widely used construction material on the planet, and its production accounts for nearly 8% of global CO₂ emissions,” said Rahbar. “What our team has developed is a practical, scalable alternative that doesn’t just reduce emissions — it actually captures carbon. Producing a single cubic meter of ESM sequesters more than 6 kilograms of CO₂, compared to the 330 kilograms emitted by conventional concrete.”

Built for Real-World Use

ESM combines fast curing with adjustable strength and full recyclability. These qualities make it well suited for practical applications such as roof decks, wall panels, and modular building systems. The material can also be repaired, which may lower long-term construction costs and significantly reduce how much waste ends up in landfills.

“If even a fraction of global construction shifts toward carbon-negative materials like ESM, the impact could be enormous,” added Rahbar.

Broad Potential Across Industries

Beyond standard construction, the material could support affordable housing, climate-resilient infrastructure, and disaster recovery efforts. Lightweight components that can be produced quickly may help speed rebuilding after extreme events. Because ESM relies on low-energy manufacturing and renewable biological inputs, it also supports broader goals tied to carbon-neutral infrastructure and circular manufacturing systems.

The discovery, made by researchers at UVA Health and Mount Sinai, could help doctors spot high-risk patients earlier and open the door to new treatments aimed at preventing or slowing heart failure in people with kidney disease.

“Kidney and heart disease can develop silently, so they are often discovered only after damage has already been done,” said researcher Uta Erdbrügger, MD, an internal medicine physician-scientist with the University of Virginia School of Medicine’s Division of Nephrology. “Our findings can help to identify patients at risk for heart failure earlier, enabling earlier treatment and improved outcomes.”

Heart Failure Risk in Chronic Kidney Disease

Chronic kidney disease affects more than 1 in 7 Americans, or roughly 35 million people in the United States, according to the National Institutes of Health. The condition is especially common among people with other health issues. About 1 in 3 patients with diabetes and around 1 in 5 people with hypertension (high blood pressure) also have kidney disease.

Doctors have long known that chronic kidney disease and cardiovascular disease are closely connected, with more severe kidney damage linked to worse heart outcomes. However, understanding exactly why this happens has been difficult. Many patients share overlapping risk factors such as obesity and high blood pressure, making it hard to determine whether the kidneys themselves play a direct role in harming the heart.

A Kidney-Specific Cause Identified

Until now, researchers had not been able to identify a kidney-specific factor that directly damages the heart. The new study led by Erdbrügger and her colleagues points to a clear culprit. Diseased kidneys release tiny particles known as “circulating extracellular vesicles” into the bloodstream.

Extracellular vesicles are produced by nearly all cells and normally act as messengers, transporting proteins and other materials between cells. In people with chronic kidney disease, however, these vesicles carry small, non-coding RNA called miRNA that the researchers found to be toxic to heart tissue.

Lab and Patient Evidence

In laboratory mice, preventing these extracellular vesicles from circulating led to noticeable improvements in heart function and reduced signs of heart failure. The research team also analyzed blood plasma samples from people with chronic kidney disease and from healthy individuals. Harmful extracellular vesicles were found in patients with kidney disease but not in healthy volunteers.

“Doctors always wondered how organs such as the kidney and heart communicate with each other. We show that EVs from the kidney can travel to the heart and be toxic,” Erdbrügger said. “We are just at the beginning to understand this communication.”

Toward Earlier Detection and New Treatments

The findings suggest that a blood test could one day be developed to identify people with chronic kidney disease who face the highest risk of serious heart problems. Researchers may also be able to design therapies that block or neutralize these circulating extracellular vesicles, reducing their damaging effects on the heart.

“Our hope is to develop novel biomarkers and treatment options for our kidney patients at risk for heart disease,” Erdbrügger said. “Potentially our work will improve precision medicine for CKD and Heart failure patients, so that each patient gets the exact treatment they need.”

Advancing Extracellular Vesicle Research

To help move this field forward, Erdbrügger is organizing a hands-on workshop for UVA scientists focused specifically on extracellular vesicle research. The five-day workshop begins Feb. 7.

Finding answers to the most pressing medical mysteries and developing new treatments for complex diseases are key goals of UVA’s new Paul and Diane Manning Institute of Biotechnology. The institute is designed to speed the transition from laboratory discoveries to real-world therapies that can save lives.

Findings Published

The research findings were published in the scientific journal Circulation. The article is open access, meaning it is available to read for free.

The research team included Xisheng Li Nikhil Raisinghani, Alex Gallinat, Carlos G. Santos-Gallego, Shihong Zhang, Sabrina La Salvia, Seonghun Yoon, Hayrettin Yavuz, Anh Phan, Alan Shao, Michael Harding, David Sachs, Carol Levy, Navneet Dogra, Rupangi Vasavada, Nicole Dubois, Erdbrügger and Susmita Sahoo. The scientists reported no financial conflicts of interest.

The study was funded by the National Institute of Health through grants HL140469, HL124187, HL148786, R01DK125856, 1-INO-2025-1704-A-N, R21AG07848, and R01DK133598.

Most available treatments focus on easing symptoms, but their benefits often fade over time. Now, researchers at Case Western Reserve University have identified a specific biological pathway that contributes to the underlying damage caused by the disease.

A Harmful Protein Chain Reaction

The study, recently published in Molecular Neurodegeneration, explains how the buildup of toxic proteins inside brain cells leads to the death of neurons responsible for movement, a hallmark of Parkinson’s disease.

“We’ve uncovered a harmful interaction between proteins that damages the brain’s cellular powerhouses, called mitochondria,” said Xin Qi, the study’s senior author and Jeanette M. and Joseph S. Silber Professor of Brain Sciences at the Case Western Reserve School of Medicine. “More importantly, we’ve developed a targeted approach that can block this interaction and restore healthy brain cell function.”

After three years of investigation, the team discovered that alpha-synuclein, a protein known to accumulate in Parkinson’s disease, abnormally binds to an enzyme called ClpP. This enzyme normally helps maintain cellular health, but the interaction disrupts its function.

Damage to the Brain’s Energy Supply

When alpha-synuclein interferes with ClpP, mitochondria begin to fail. These structures act as the cell’s energy generators, and their impairment triggers widespread neurodegeneration and brain cell loss. Experiments across several research models also showed that this molecular interaction speeds up the progression of Parkinson’s disease.

To counter this process, the researchers developed a treatment known as CS2. The compound is designed to block the damaging protein interaction and help mitochondria recover their normal function. CS2 acts as a decoy, drawing alpha-synuclein away from ClpP and preventing it from harming the cell’s energy systems.

In multiple study models, including human brain tissue, patient-derived neurons and mice models, CS2 reduced brain inflammation and led to improvements in movement and cognitive performance.

Targeting the Disease, Not Just Symptoms

“This represents a fundamentally new approach to treating Parkinson’s disease,” said Di Hu, a research scientist in the School of Medicine’s Department of Physiology and Biophysics. “Instead of just treating the symptoms, we’re targeting one of the root causes of the disease itself.”

The breakthrough builds on Case Western Reserve’s strengths in mitochondrial biology and neurodegenerative disease research, along with its collaborative environment and advanced experimental models. These resources helped translate basic biological insights into a potential therapeutic strategy.

Next Steps Toward Clinical Use

Over the next five years, the team aims to move the discovery closer to human clinical trials. Planned efforts include refining the drug for use in people, expanding safety and effectiveness testing, identifying key molecular biomarkers tied to disease progression, and advancing toward patient-focused treatments.

“One day,” Qi said, “we hope to develop mitochondria-targeted therapies that will enable people to regain normal function and quality of life, transforming Parkinson’s from a crippling, progressive condition into a manageable or resolved one.”

The research, published on January 7 in Cell Stem Cell, removes a major barrier that has slowed the development, affordability, and large-scale production of cell therapies. By solving this problem, the work could help make off-the-shelf treatments more accessible and effective for conditions such as cancer, infectious diseases, autoimmune disorders, and more.

“Engineered cell therapies are transforming modern medicine,” said co-senior author Dr. Peter Zandstra, professor and director of the UBC School of Biomedical Engineering. “This study addresses one of the biggest challenges in making these lifesaving treatments accessible to more people, showing for the first time a reliable and scalable way to grow multiple immune cell types.”

The Promise and Limits of Living Drugs

Over the past several years, engineered cell therapies such as CAR-T treatments have produced dramatic, sometimes lifesaving results for people with cancers that were once considered untreatable. These therapies work by reprogramming a patient’s immune cells to recognize and destroy disease, effectively turning those cells into ‘living drugs’.

Even with their success, cell therapies remain costly, complex to manufacture, and out of reach for many patients around the world. One key reason is that most existing treatments rely on a patient’s own immune cells, which must be collected and specially prepared over several weeks for each individual.

“The long-term goal is to have off-the-shelf cell therapies that are manufactured ahead of time and on a larger scale from a renewable source like stem cells,” said co-senior author Dr. Megan Levings, a professor of surgery and biomedical engineering at UBC. “This would make treatments much more cost-effective and ready when patients need them.”

Cancer cell therapies are most effective when two types of immune cells work together. Killer T cells directly attack infected or cancerous cells. Helper T cells, which act as the immune system’s conductors — detecting health threats, activating other immune cells and sustaining the immune responses over time — play a central coordinating role.

While scientists have made progress using stem cells to create killer T cells in the lab, they have not been able to reliably generate helper T cells until now.

“Helper T cells are essential for a strong and lasting immune response,” said Dr. Levings. “It’s critical that we have both to maximize the efficacy and flexibility of off-the-shelf therapies.”

A Key Advance Toward Stem Cell Based Immune Therapies

In the new study, the UBC research team addressed this long-standing challenge by carefully adjusting biological signals that guide how stem cells develop. This approach allowed them to precisely control whether stem cells became helper T cells or killer T cells.

The scientists found that a developmental signal known as Notch plays an important but time-sensitive role in immune cell formation. Notch is necessary early in development, but if the signal stays active for too long, it blocks the formation of helper T cells.

“By precisely tuning when and how much this signal is reduced, we were able to direct stem cells to become either helper or killer T cells,” said co-first author Dr. Ross Jones, a research associate in the Zandstra Lab. “We were able to do this in controlled laboratory conditions that are directly applicable in real-world biomanufacturing, which is an essential step toward turning this discovery into a viable therapy.”

The team also confirmed that the lab-grown helper T cells functioned like real immune cells, not just in appearance but in behavior. The cells showed signs of full maturity, carried a wide variety of immune receptors, and were able to develop into specialized subtypes with distinct immune roles.

“These cells look and act like genuine human helper T cells,” said co-first author Kevin Salim, a UBC PhD student in the Levings Lab. “That’s critical for future therapeutic potential.”

Researchers say the ability to generate both helper and killer T cells, and to carefully control their balance, could greatly improve the effectiveness of stem cell-derived immune therapies.

“This is a major step forward in our ability to develop scalable and affordable immune cell therapies,” said Dr. Zandstra. “This technology now forms the foundation for testing the role of helper T cells in supporting the elimination of cancer cells and generating new types of helper T cell-derived cells, such as regulatory T cells, for clinical applications.”